Uploaded by emma.kiene07

diabetes notecards

advertisement
Risk factors for T1 diabetes



Symptoms for TI diabetes










Risk factors for T2 diabetes




Symptoms of T2 diabetes










Common in young people
Pancreas does not make insulin
No insulin production
Polyuria- increase urination
Polydipsia- increase thirst
Polyphagia- increase hunger
Weight loss
Fatigue
Increase frequency of infections
Rapid onset
Insulin dependent
Familial tendency
Peak incidence from 10-15 years
Most prevalent type of diabetes
Increasing in children
Obesity, poor diet, and lack of exercise
Insulin is produced in insufficient amounts or
poorly used
Sedentary lifestyle
Familial tendency
Average age of 50 years
Hx of increase BP
Fatigue, decrease energy
Ovese
Recurrent infections
Polyuria
Polydipsia
FBS- >126
T1 meal planning
based on individual, usual food intake and balanced with
insulin and exercise
T2 meal planning
goal is to achieve acceptable glucose, lipid, and blood
pressure goals
Carbohydrates
primary source of energy (min 130g/day)
Fats
provides energy and carries fat-soluble vitamins
Protein
should contribute 15-20% of total calories consumed
Alcohol
inhibits gluconeogenesis, can cause severe hypoglycemia
if patient taking oral hypoglycemic medications or insulin
Carbohydrate counting
Each diabeteic bases their insulin doses off of the
carbs that they ingest and have different ratios
1 unit of insulin is how many
carbs
30 carbs
4 units of insulin is how many
carbs
15 carbs
How does exercise help with
diabetes?
When should a person
exercise?
Delayed exercise induced
hypoglycemia
What are the 4 M’s of
diabetes for patient
education?
lowers blood glucose level
1 hour after meal and check blood and glucose level
before and after exercising
May occur several hours after completion of exercise




Labs for diagnosing diabetes




Hemoglobin A1C





Ideal goal for hemoglobin A1C

Medication
Monitoring
Meal planning
Motion (exercise)
Fasting plasma glucose level >126 mg/dl
Random plasma glucose >200 mg/dl +
manifestations of diabetes
Two hour oral glucose tolerance test level >200
mg/dl using glucose load of 75g
A1C of 6.5% or higher
Best indicator of glucose level
Shows amount of glucose that has been attached
to hemoglobin molecule over lifespan of molecule
Indicates glucose control for past 90-120 days
Determines glycemic levels overtime
Used to monitor and make changes in treatments
6.5%-7.0% or less for patient diagnosed with
diabetes and being treated
Normal A1C level

Below 5.7%
Prediabetes A1C level

5.7-6.4%
Diabetes A1C level

6.5% or above
Complications of hyperglycemia

Polyuria
Glycosuria
Polydipsia
Weight loss
Malaise and fatigue
Stressful situations





polyuria
hyperglycemia acts as osmotic diuretic
glycosuria
renal threshold for glucose: 180 mg/dl
polydipsia
thirst from dehydration; from polyuria
polyphagia
hunger and eats more; since cell cannot utilize
glucose
Stressful situations
Angiopathy
body’s response to illness and stress is to produce
glucose which can result in hyperglycemia






Diabetic Retinopathy

Disease of small blood vessels
Specific to diabetes
Endothelial dysfunction
Thickening of the basement membrane in the
capillaries and arterioles
Seen prior to or with onset of diabetes
Lose sensation in areas affected
Microvascular damage to the retina due to
 Chronic hyperglycemia
 Nephropathy
 HTN
 Microaneurysms form
 Capillary wall week
 Retinal edema
 Need annual eye exams
Nephropathy
Risk factors of Nephropathy
Microvascular complication associated with damage
that supply glomeruli of kidney




Increase risk of infection
Increase risk of injury
Infection and delayed wound healing
 High glucose in blood vessels
 BV become narrow due to scarring
 Elevated BS level= decreased function of RBC
 Persistent glycosuria




Neuropathy
Sensory Neuropathy
Foot care of diabteic patients
Due to decreased tactile sensation
Caution about potential sources of injury to
feet
Teach patient to inspect inside of shoes for
foreign objects
Related to hypoglycemia
 Monitor for s/s of hypoglycemia
 Teach patient to have simple carbs
available
Nerve damage due to metabolic disturbances
associated with diabetes


Autonomic Neuropathy
HTN
Genetic predisposition
Smoking
Chronic hyperglycemia
Loss of protective sensation in lower
extremities
Exam feet-avoid injury, proper footwear,
proper nail care
Can affect nearly all body systems: hypoglycemic
unawareness, postural hypotension, painless MI





Examine feet daily
Wash feet with warm water and mild soap
Pat dry, don't rub
Keep feet from drying and cracking
Extra care with toenail care
Nursing management of pt with
DM in ambulatory and home care
settings








Methods to protect the pt with DM from
injury and infections
Monitor blood glucose
 Increase BG= increase UO
Monitor urine output amount and presence of ketones
Monitor IV fluids- insulin therapy- electrolyte
imbalance
 Potassium is needed to move insulin into the
cells
Assess renal and cardiac status
 Telemetry monitor because and increase in
potassium can affect the heart
Assess for neuro changes/consciousness
Cardiac monitoring
Frequent vital signs (BP, HR, Temp)
Reassure patient



Hypoglycemia



Symptoms of hypoglycemia



Treatment of hypoglycemia



To influence go shoe wear and
protection of feet
Don’t keep feet dry or too
moisturized
Monitor glucose levels before and
after exercise
too much insulin for available
glucose
Less than 70 mg/dl
Sudden shift and fall of glucose
Result of epinephrine
Nervousness, irritability,
increased heart rate, diaphoresis,
impaired mental status
TIRED: tachycardia, irritability,
restless, excessive hunger,
diaphoresis, depression
Simple carbohydrate foods; if patient
is alert
Commercial gels or glucose tabletsalert b/c choking hazard
If patients had decreased LOC


Diabetic Ketoacidosis





Causes of diabetic ketoacidosis




Process of diabetic ketoacidosis
Clinical manifestations of diabetic
ketoacidosis
Ketones present
Life threatening emergency
Gross insulin deficiency
predominant problem
Most common in T1
Mortality 5-10%
Increase calories
Too little insulin
Stress from physical illnessinfection
Undiagnosed DM
glucose cannot be used > cellular
starvation > breakdown of protein and
fats > free fatty acids > ketones








Diagnostic test of diabetic ketoacidosis
Glucagon IV or IM
D50 IV push in acute situation




lethargy/weakness
Severe dehydration
Abdominal pain
Anorexia
Vomiting
kussmaul/labored breathing, high
rate
Urinary frequency + thirst
Breath odor (ketones)- fruity
BG >300 mg/dl
pH <7.3
HCO3 < 15 mEq/L
Positive ketones (blood & urine)
Treatment of diabetic ketoacidosis





Insulin drip rate
Hyperglycemic Hyperosmolar Syndrome
(HHS)
0.1u/kg/hr







Lab values of HHS
ABCs always first priority
IV access + NS bolus until BP is
stable
Insulin drip @ 0.1u/kg/hr
Correct electrolyte imbalance
Potassium may be initially high due
to hemoconcentration- will
decrease as fluids are given and
insulin drives potassium into cells



Life threatening emergency
Occurs in patients with type 2
Affects predominantly the elderly
Characterized by very high blood
glucose levels
 Without or minimal ketones
Mortality is high
Occurs in patients that are able to
produce some insulin but not
enough to prevent hyperglycemia
Produces fewer symptoms in early
stages- blood sugar can raise quite
high before symptoms are seen
Blood glucose- >600 mg/dl
Increase in serum osmolarity
No or very minimal ketones in both
blood and urine
 Medical emergency
 HHS usually requires
greater volumes of fluid
replacement
 Careful to avoid fluid
overload
Insulin
Insulin syringes
short acting before meals and long acting
once a day




Sites of admin for insulin
Lipodystrophy
Insulin pump

Fastest absorption is in the
abdomen, then arm, thigh, and
buttock
bumps dents in skin from repeated
injections






Sliding Scale
Can only be used to give insulin
Measured in units not mls
Insulin is considered high hazard
medication- needs to be double
checked by 2 RNs
Administered subcutaneously at
45 (for skinny), 60, or 90 degree
angle in to subcutaneous tissue- do
not aspirate


Connected with plastic tube inserted into
subcutaneous tissue in abdominal wall
Delivers rapid-acting insulin, continuously;
24 hours at a “basal rate”
Provides tight glucose control- able to
increase amounts during meals, exercise
Patient must check blood sugars more
often 4-8 times a day
Insertion site must be checked frequently
Administration set must be changed every
2-3 days: to new sites as well
Sometimes referred to as
corrective insulin
Always use short acting insulin
Insulin syringe
Oral agents of insulin





Metformin MOA
Metformin SE
↓ Rate of hepatic glucose production. ↑ Insulin sensitivity.
Improves glucose uptake by tissues, especially muscles



Glipizide MOA
Glipizide SE
Sitagliptin SE
Diarrhea
lactic acidosis.
Must be held 1–2 days before IV contrast media given
and for 48 hr after
Stimulates release of insulin from pancreatic islets. ↓
Glycogenolysis and gluconeogenesis. Enhances cellular
sensitivity to insulin


Sitagliptin MOA
Used for type 2 diabetes
Used in combination with each other
Many time used with daily glargine (Lantus) or other
long acting insulin
Elevated sugars covered by rapid or short acting
Goal is to control sugar through out day with oral agents
and possibly some insulin regimen
Weight gain
hypoglycemia
Enhances activity of incretins. Stimulates release of insulin
from pancreatic β-cells. ↓ Hepatic glucose production


Pancreatitis
allergic reactions
Exenatide MOA
Exenatide SE
Stimulates release of insulin, ↓ glucagon secretion, and slow
gastric emptying. ↑ Satiety





Liraglutide MOA
Liraglutide SE
Stimulates release of insulin, ↓ glucagon secretion, and slow
gastric emptying. ↑ Satiety





Rationale behind carb
counting
Nausea
Vomiting
Hypoglycemia
Diarrhea
headache
Nausea
Vomiting
Hypoglycemia
Diarrhea
headache
Because carbs turn into sugars (glucose) and insulin is needed
to break them down
Why focus on carbs vs.
fats and proteins
Fats and proteins are stored more easily in the body through
the liver and adipose tissue, while carbs have to have access to
cells by insulin to be able to go into the cells
Different types of
carbs and how they
affect glucose level
There are carbs simple and complex- simple are broken down in
the mouth and these are carbs like starches and simple sugars.
While more complex are broken down in the stomach and
absorbed in the intestines
How to adjust
medications:
Amiodarone
(Cordarone)
Medications should be adjusted based on the effect that
carbs have on the individual and there insulin ratio as well as
the sliding scale (correction dose)


Classification: antiarrhythmic clas 3
MOA: prolongs action potential and refractory period.
Inhibits adrenergic stimulation. Slows the sinus rate,
increases PR and QT interval, and decreases peripheral
vascular resistance (vasodilation), suppresses
arrhythmias
SE of amiodarone

















Dizziness
Fatigue
Malaise,
corneal microdeposits
Bradycardia
Hypotension
Anorexia
Constipation
N/V
Photosensitivity
Hypothyroidism
Ataxia
involuntary movement
Paresthesia
peripheral neuropathy
poor coordination
tremor
Furosemide

Classification: loop diuretic
MOA: inhibits the reabsorption of sodium and chloride
from the loop of Henle and distal renal tubule.
Increases renal excretion of water, sodium, chloride,
magnesium, potassium, and calcium- used to mobilize
fluid

SE of furosemide






Spironolactone


SE of
spironolactone







Increased urination
thirst, muscle cramps
Itching
Weakness
Dizziness
diarrhea
Classification: potassium sparing diuretics
MOA: acts in the renal distal tubule and collecting
ducts decreasing the reabsorption of sodium and
decreasing the excretion of potassium
Diarrhea
Nausea
Vomiting
leg cramps
Headaches
Dizziness
drowsiness
Corticosteroids


SE of
corticosteroids






Doxazosin


SE of doxazosin







Calcitriol


SE of calcitriol








Levothyroxine


Classification: anti-inflammatory
MOA: binding to intracellular receptors which then act to
modulate gene transcription in target tissues
Glaucoma
fluid retention
high BP
Confusion
mood swings
delirium
Classification: alpha-blocker
MOA: Relieves the symptoms of BPH by relaxing the muscles
of the bladder and prostate
Headache
Tiredness
Swelling
SOB
weight gain
abnormal vision
runny nose
Class: Vitamin D analog
MOA: Works by helping the body to use more calcium found
in foods or supplements and regulating the body’s production
of parathyroid
Abdominal pain
bone pain
Apathy
BUN and creatinine increased
cardiac arrhythmia
changes in behavior
Constipation
decreased libido
Class: thyroid hormone
MOA: treat hypothyroidism
SE of
levothyroxine










Fatigue
increased appetite
weight loss
heat intolerance
Headache
Hyperactivity
Nervousness
Anxiety
Tremors
sweating
Download